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  • 11
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    Primary structure and functional expression of the beta 1 subunit of the rat brain sodium channel (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-05-08
    Description: Voltage-sensitive sodium channels are responsible for the initiation and propagation of the action potential and therefore are important for neuronal excitability. Complementary DNA clones encoding the beta 1 subunit of the rat brain sodium channel were isolated by a combination of polymerase chain reaction and library screening techniques. The deduced primary structure indicates that the beta 1 subunit is a 22,851-dalton protein that contains a single putative transmembrane domain and four potential extracellular N-linked glycosylation sites, consistent with biochemical data. Northern blot analysis reveals a 1,400-nucleotide messenger RNA in rat brain, heart, skeletal muscle, and spinal cord. Coexpression of beta 1 subunits with alpha subunits increases the size of the peak sodium current, accelerates its inactivation, and shifts the voltage dependence of inactivation to more negative membrane potentials. These results indicate that the beta 1 subunit is crucial in the assembly, expression, and functional modulation of the heterotrimeric complex of the rat brain sodium channel.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Isom, L L -- De Jongh, K S -- Patton, D E -- Reber, B F -- Offord, J -- Charbonneau, H -- Walsh, K -- Goldin, A L -- Catterall, W A -- NS15751/NS/NINDS NIH HHS/ -- NS25704/NS/NINDS NIH HHS/ -- NS26729/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 May 8;256(5058):839-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1375395" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blotting, Northern ; Brain/*physiology ; Cloning, Molecular ; DNA/genetics/isolation & purification ; Female ; Kinetics ; Macromolecular Substances ; Membrane Potentials ; Molecular Sequence Data ; Oocytes/physiology ; Polymerase Chain Reaction/methods ; Protein Conformation ; RNA/genetics/isolation & purification ; RNA, Messenger/genetics ; Rats ; Sodium Channels/*genetics/*physiology ; Voltage-Gated Sodium Channel beta-1 Subunit ; Xenopus
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    Reward-predictive cues enhance excitatory synaptic strength onto midbrain dopamine neurons (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-20
    Description: Using sensory information for the prediction of future events is essential for survival. Midbrain dopamine neurons are activated by environmental cues that predict rewards, but the cellular mechanisms that underlie this phenomenon remain elusive. We used in vivo voltammetry and in vitro patch-clamp electrophysiology to show that both dopamine release to reward predictive cues and enhanced synaptic strength onto dopamine neurons develop over the course of cue-reward learning. Increased synaptic strength was not observed after stable behavioral responding. Thus, enhanced synaptic strength onto dopamine neurons may act to facilitate the transformation of neutral environmental stimuli to salient reward-predictive cues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2613864/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2613864/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stuber, Garret D -- Klanker, Marianne -- de Ridder, Bram -- Bowers, M Scott -- Joosten, Ruud N -- Feenstra, Matthijs G -- Bonci, Antonello -- DA015096/DA/NIDA NIH HHS/ -- DA021937/DA/NIDA NIH HHS/ -- R01 DA015096/DA/NIDA NIH HHS/ -- R01 DA015096-06/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 19;321(5896):1690-2. doi: 10.1126/science.1160873.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ernest Gallo Clinic and Research Center, Department of Neurology, University of California, San Francisco, Emeryville, CA 94608, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18802002" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conditioning (Psychology) ; Cues ; Dopamine/*physiology ; Excitatory Postsynaptic Potentials ; *Learning ; Long-Term Potentiation ; Male ; Mesencephalon/cytology/*physiology ; Neurons/*physiology ; Nucleus Accumbens/*physiology ; Patch-Clamp Techniques ; Rats ; Receptors, AMPA/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; *Reward ; Signal Transduction ; Synapses/*physiology ; Synaptic Transmission
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    Activation of corticotropin-releasing factor in the limbic system during cannabinoid withdrawal (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-27
    Description: Corticotropin-releasing factor (CRF) has been implicated in the mediation of the stress-like and negative affective consequences of withdrawal from drugs of abuse, such as alcohol, cocaine, and opiates. This study sought to determine whether brain CRF systems also have a role in cannabinoid dependence. Rats were treated daily for 2 weeks with the potent synthetic cannabinoid HU-210. Withdrawal, induced by the cannabinoid antagonist SR 141716A, was accompanied by a marked elevation in extracellular CRF concentration and a distinct pattern of Fos activation in the central nucleus of the amygdala. Maximal increases in CRF corresponded to the time when behavioral signs resulting from cannabinoid withdrawal were at a maximum. These data suggest that long-term cannabinoid administration alters CRF function in the limbic system of the brain, in a manner similar to that observed with other drugs of abuse, and also induces neuroadaptive processes that may result in future vulnerability to drug dependence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rodriguez de Fonseca, F -- Carrera, M R -- Navarro, M -- Koob, G F -- Weiss, F -- DA 08426/DA/NIDA NIH HHS/ -- DK26741/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):2050-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Instituto Complutense de Drogodependencias, Departamento de Psicobiologia, Facultad de Psicologia, Universidad Complutense de Madrid, 28223 Madrid, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9197270" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/drug effects/*metabolism ; Animals ; Anxiety/chemically induced ; Behavior, Animal/drug effects ; Brain/drug effects/*metabolism ; Corticosterone/blood ; Corticotropin-Releasing Hormone/*metabolism ; Dronabinol/adverse effects/*analogs & derivatives/antagonists & ; inhibitors/pharmacology ; Male ; Microdialysis ; Piperidines/pharmacology ; Proto-Oncogene Proteins c-fos/analysis ; Pyrazoles/pharmacology ; Rats ; Rats, Wistar ; Receptors, Cannabinoid ; Receptors, Drug/antagonists & inhibitors ; Substance Withdrawal Syndrome/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    Calorie restriction promotes mammalian cell survival by inducing the SIRT1 deacetylase (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-06-19
    Description: A major cause of aging is thought to result from the cumulative effects of cell loss over time. In yeast, caloric restriction (CR) delays aging by activating the Sir2 deacetylase. Here we show that expression of mammalian Sir2 (SIRT1) is induced in CR rats as well as in human cells that are treated with serum from these animals. Insulin and insulin-like growth factor 1 (IGF-1) attenuated this response. SIRT1 deacetylates the DNA repair factor Ku70, causing it to sequester the proapoptotic factor Bax away from mitochondria, thereby inhibiting stress-induced apoptotic cell death. Thus, CR could extend life-span by inducing SIRT1 expression and promoting the long-term survival of irreplaceable cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Haim Y -- Miller, Christine -- Bitterman, Kevin J -- Wall, Nathan R -- Hekking, Brian -- Kessler, Benedikt -- Howitz, Konrad T -- Gorospe, Myriam -- de Cabo, Rafael -- Sinclair, David A -- AG19719-03/AG/NIA NIH HHS/ -- AG19972-02/AG/NIA NIH HHS/ -- F32 CA097802/CA/NCI NIH HHS/ -- P01 AG027916/AG/NIA NIH HHS/ -- R01 AG019719/AG/NIA NIH HHS/ -- R01 AG019972/AG/NIA NIH HHS/ -- R01 AG028730/AG/NIA NIH HHS/ -- R01 GM068072/GM/NIGMS NIH HHS/ -- R37 AG028730/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2004 Jul 16;305(5682):390-2. Epub 2004 Jun 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15205477" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Adipose Tissue/metabolism ; Alleles ; Animals ; Antigens, Nuclear/metabolism ; *Apoptosis ; *Caloric Restriction ; Cell Line ; *Cell Survival ; DNA-Binding Proteins/metabolism ; Histone Deacetylases/genetics/*metabolism ; Humans ; Insulin/metabolism/pharmacology ; Insulin-Like Growth Factor I/metabolism/pharmacology ; Kidney/metabolism ; Liver/metabolism ; Male ; Mitochondria/metabolism ; Mutation ; Proto-Oncogene Proteins/metabolism ; *Proto-Oncogene Proteins c-bcl-2 ; RNA, Small Interfering ; Rats ; Rats, Inbred F344 ; Sirtuin 1 ; Sirtuins/genetics/*metabolism ; bcl-2-Associated X Protein
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    A conditional knockout resource for the genome-wide study of mouse gene function (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-06-17
    Description: Gene targeting in embryonic stem cells has become the principal technology for manipulation of the mouse genome, offering unrivalled accuracy in allele design and access to conditional mutagenesis. To bring these advantages to the wider research community, large-scale mouse knockout programmes are producing a permanent resource of targeted mutations in all protein-coding genes. Here we report the establishment of a high-throughput gene-targeting pipeline for the generation of reporter-tagged, conditional alleles. Computational allele design, 96-well modular vector construction and high-efficiency gene-targeting strategies have been combined to mutate genes on an unprecedented scale. So far, more than 12,000 vectors and 9,000 conditional targeted alleles have been produced in highly germline-competent C57BL/6N embryonic stem cells. High-throughput genome engineering highlighted by this study is broadly applicable to rat and human stem cells and provides a foundation for future genome-wide efforts aimed at deciphering the function of all genes encoded by the mammalian genome.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3572410/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3572410/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Skarnes, William C -- Rosen, Barry -- West, Anthony P -- Koutsourakis, Manousos -- Bushell, Wendy -- Iyer, Vivek -- Mujica, Alejandro O -- Thomas, Mark -- Harrow, Jennifer -- Cox, Tony -- Jackson, David -- Severin, Jessica -- Biggs, Patrick -- Fu, Jun -- Nefedov, Michael -- de Jong, Pieter J -- Stewart, A Francis -- Bradley, Allan -- 077188/Wellcome Trust/United Kingdom -- U01-HG004080/HG/NHGRI NIH HHS/ -- Wellcome Trust/United Kingdom -- England -- Nature. 2011 Jun 15;474(7351):337-42. doi: 10.1038/nature10163.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK. skarnes@sanger.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21677750" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Computational Biology ; Embryonic Stem Cells/cytology/metabolism ; *Gene Deletion ; Gene Knockout Techniques/*methods ; Genes/*genetics ; Genes, Lethal/genetics ; Genetic Association Studies/*methods ; Genetic Vectors/genetics ; Genome/*genetics ; Genomics ; Genotype ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Knockout/*genetics ; Mutagenesis, Insertional/methods ; Phenotype ; Polymerase Chain Reaction ; Rats
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 16
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    Retinoic acid stimulates regeneration of mammalian auditory hair cells (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-30
    Description: Sensorineural hearing loss resulting from the loss of auditory hair cells is thought to be irreversible in mammals. This study provides evidence that retinoic acid can stimulate the regeneration in vitro of mammalian auditory hair cells in ototoxic-poisoned organ of Corti explants in the rat. In contrast, treatment with retinoic acid does not stimulate the formation of extra hair cells in control cultures of Corti's organ. Retinoic acid-stimulated hair cell regeneration can be blocked by cytosine arabinoside, which suggests that a period of mitosis is required for the regeneration of auditory hair cells in this system. These results provide hope for a recovery of hearing function in mammals after auditory hair cell damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lefebvre, P P -- Malgrange, B -- Staecker, H -- Moonen, G -- Van de Water, T R -- DC00088/DC/NIDCD NIH HHS/ -- NS07098/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 30;260(5108):692-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Physiology and Pathophysiology, University of Liege, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8480180" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytarabine/pharmacology ; Hair Cells, Auditory/*drug effects/physiology/ultrastructure ; Microscopy, Electron ; Neomycin/toxicity ; Organ Culture Techniques ; Organ of Corti/*drug effects/physiology/ultrastructure ; Rats ; Regeneration/*drug effects ; Tretinoin/*pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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    Modulation of chemotropism in the developing spinal cord by substance P (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-02-10
    Description: Developing axons find their targets through direct contact with cues in the extracellular environment and in response to gradients of diffusible factors. The floor plate, a neuroepithelial structure, guides developing commissural axons in the spinal cord by release of chemoattractants. Floor plate cells express neurokinin-1 receptors, and a transiently appearing subpopulation of commissural axons contains substance P, the neuropeptide ligand for this receptor. Substance P increases the amount of axon outgrowth from dorsal horn explants cocultured with floor plate explants. Results of experiments with embryonic rats suggest that substance P released from pioneering neuronal pathways may regulate the release of chemoattractants from floor plate cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉De Felipe, C -- Pinnock, R D -- Hunt, S P -- New York, N.Y. -- Science. 1995 Feb 10;267(5199):899-902.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neurobiology, Medical Research Council, Cambridge, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7531367" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Axons/physiology/ultrastructure ; Calcium/metabolism ; Central Nervous System/chemistry/cytology/*embryology/metabolism ; Chemotactic Factors/*metabolism ; Culture Techniques ; Neurons/chemistry/*physiology/ultrastructure ; Rats ; Receptors, Neurokinin-1/analysis/metabolism ; Spinal Cord/cytology/*embryology ; Substance P/analysis/*metabolism/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    Regulation of a neuronal form of focal adhesion kinase by anandamide (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-09-20
    Description: Anandamide is an endogenous ligand for central cannabinoid receptors and is released after neuronal depolarization. Anandamide increased protein tyrosine phosphorylation in rat hippocampal slices and neurons in culture. The action of anandamide resulted from the inhibition of adenylyl cyclase and cyclic adenosine 3', 5'-monophosphate-dependent protein kinase. One of the proteins phosphorylated in response to anandamide was an isoform of pp125-focal adhesion kinase (FAK+) expressed preferentially in neurons. Focal adhesion kinase is a tyrosine kinase involved in the interactions between the integrins and actin-based cytoskeleton. Thus, anandamide may exert neurotrophic effects and play a role in synaptic plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Derkinderen, P -- Toutant, M -- Burgaya, F -- Le Bert, M -- Siciliano, J C -- de Franciscis, V -- Gelman, M -- Girault, J A -- New York, N.Y. -- Science. 1996 Sep 20;273(5282):1719-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM U 114, Chaire de Neuropharmacologie, College de France, 11 place Marcelin Berthelot, 75231 Paris cedex 05, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8781236" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclase Inhibitors ; Adenylyl Cyclases/metabolism ; Amino Acid Sequence ; Animals ; Arachidonic Acid/pharmacology ; Arachidonic Acids/*pharmacology ; Cell Adhesion Molecules/*metabolism ; Cell Line ; Cells, Cultured ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Endocannabinoids ; Focal Adhesion Kinase 1 ; Focal Adhesion Protein-Tyrosine Kinases ; Hippocampus/drug effects/*enzymology ; In Vitro Techniques ; Molecular Sequence Data ; Neuronal Plasticity/drug effects ; Neurons/drug effects/*enzymology ; Phosphorylation ; Phosphotyrosine/metabolism ; Polyunsaturated Alkamides ; Prosencephalon ; Protein-Tyrosine Kinases/*metabolism ; Rats ; Receptors, Cannabinoid ; Receptors, Drug/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 19
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    The antidepressant fluoxetine restores plasticity in the adult visual cortex (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-04-19
    Description: We investigated whether fluoxetine, a widely prescribed medication for treatment of depression, restores neuronal plasticity in the adult visual system of the rat. We found that chronic administration of fluoxetine reinstates ocular dominance plasticity in adulthood and promotes the recovery of visual functions in adult amblyopic animals, as tested electrophysiologically and behaviorally. These effects were accompanied by reduced intracortical inhibition and increased expression of brain-derived neurotrophic factor in the visual cortex. Cortical administration of diazepam prevented the effects induced by fluoxetine, indicating that the reduction of intracortical inhibition promotes visual cortical plasticity in the adult. Our results suggest a potential clinical application for fluoxetine in amblyopia as well as new mechanisms for the therapeutic effects of antidepressants and for the pathophysiology of mood disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maya Vetencourt, Jose Fernando -- Sale, Alessandro -- Viegi, Alessandro -- Baroncelli, Laura -- De Pasquale, Roberto -- O'Leary, Olivia F -- Castren, Eero -- Maffei, Lamberto -- New York, N.Y. -- Science. 2008 Apr 18;320(5874):385-8. doi: 10.1126/science.1150516.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Scuola Normale Superiore, Piazza dei Cavalieri, I-56100 Pisa, Italy. jf.maya@in.cnr.it〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18420937" target="_blank"〉PubMed〈/a〉
    Keywords: Amblyopia/drug therapy/physiopathology ; Animals ; Antidepressive Agents, Second-Generation/pharmacology ; Brain-Derived Neurotrophic Factor/metabolism ; Diazepam/pharmacology ; Dominance, Ocular/drug effects ; Evoked Potentials, Visual/drug effects ; Fluoxetine/administration & dosage/*pharmacology ; Long-Term Potentiation ; Long-Term Synaptic Depression ; Neuronal Plasticity/*drug effects ; Rats ; Serotonin/physiology ; Serotonin Uptake Inhibitors/*pharmacology ; Synaptic Transmission/drug effects ; Visual Cortex/*drug effects/physiology ; gamma-Aminobutyric Acid/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 20
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    A Cdc20-APC ubiquitin signaling pathway regulates presynaptic differentiation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-11-11
    Description: Presynaptic axonal differentiation is essential for synapse formation and the establishment of neuronal circuits. However, the mechanisms that coordinate presynaptic development in the brain are largely unknown. We found that the major mitotic E3 ubiquitin ligase Cdc20-anaphase promoting complex (Cdc20-APC) regulates presynaptic differentiation in primary postmitotic mammalian neurons and in the rat cerebellar cortex. Cdc20-APC triggered the degradation of the transcription factor NeuroD2 and thereby promoted presynaptic differentiation. The NeuroD2 target gene encoding Complexin II, which acts locally at presynaptic sites, mediated the ability of NeuroD2 to suppress presynaptic differentiation. Thus, our findings define a Cdc20-APC ubiquitin signaling pathway that governs presynaptic development, which holds important implications for neuronal connectivity and plasticity in the brain.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2846784/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2846784/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Yue -- Kim, Albert H -- Yamada, Tomoko -- Wu, Bei -- Bilimoria, Parizad M -- Ikeuchi, Yoshiho -- de la Iglesia, Nuria -- Shen, Jie -- Bonni, Azad -- F32 CA124028/CA/NCI NIH HHS/ -- NS041021/NS/NINDS NIH HHS/ -- NS051255/NS/NINDS NIH HHS/ -- R01 NS041021/NS/NINDS NIH HHS/ -- R01 NS041021-06/NS/NINDS NIH HHS/ -- R01 NS041021-07/NS/NINDS NIH HHS/ -- R01 NS041021-08/NS/NINDS NIH HHS/ -- R01 NS051255/NS/NINDS NIH HHS/ -- R01 NS051255-02/NS/NINDS NIH HHS/ -- R01 NS051255-03/NS/NINDS NIH HHS/ -- R01 NS051255-04/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 23;326(5952):575-8. doi: 10.1126/science.1177087.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19900895" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Vesicular Transport/genetics/metabolism ; Anaphase-Promoting Complex-Cyclosome ; Animals ; Axons/metabolism/*physiology/ultrastructure ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; Cdc20 Proteins ; Cell Cycle Proteins/genetics/*metabolism ; Cerebellar Cortex/cytology/metabolism/ultrastructure ; Gene Knockdown Techniques ; Mutant Proteins/metabolism ; Nerve Tissue Proteins/genetics/metabolism ; Neuropeptides/genetics/metabolism ; Presynaptic Terminals/*metabolism ; Rats ; *Signal Transduction ; Synapses/*metabolism ; Synapsins/metabolism ; Synaptic Vesicles/genetics/metabolism ; Ubiquitin/*metabolism ; Ubiquitin-Protein Ligase Complexes/genetics/*metabolism ; Ubiquitin-Protein Ligases/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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